Identification of factors and genes related to aluminum tolerance acquired during phosphte starvation in tobacco cells.

铝是酸性土壤中抑制植物根系生长的主要因素。然而，导致根伸长抑制的原发病变尚未确定。在细胞水平上，Al对Fe（II）依赖的脂质过氧化的刺激作用已被报道。在培养的烟草细胞中，Al和Fe（II）共同引起的脂质过氧化是导致细胞死亡的主要病变。在此条件下，缺磷（Pi）的烟草细胞表现出对Al和Fe（II）组合引起的毒性的耐受性。此外，我们还从烟草细胞中分离到了耐铝细胞株（ALT 107），本研究对缺磷细胞和ALT 107细胞中与耐铝相关的抗氧化分子进行了鉴定，结果如下：1. Pi饥饿的细胞积累类胡萝卜素色素（尤其是β-胡萝卜素）。此外，PI饥饿的细胞，以及ALT 107细胞，积累苯丙烷类化合物，包括咖啡酸的一些衍生物。苯丙烷类化合物能保护烟草细胞免受Al和Fe（II）共同引起的脂质过氧化和细胞死亡，表明苯丙烷类化合物具有抗氧化活性，能干扰脂质过氧化. PI饥饿细胞和ALT 107细胞表现出苯丙氨酸解氨酶（PAL）比活性的增加。此外，PAL的特异性抑制剂完全阻断了PI饥饿细胞和ALT 107细胞中苯丙烷类化合物的积累，表明PAL是细胞中苯丙烷类化合物积累的关键酶，这一结果提示PAL活性的调节是铝毒耐受的可能机制之一，特别是铝增强铁介导的脂质过氧化作用所引起的毒性。

Aluminum (Al) is a major factor in the inhibition of plant root growth in acid soils. However, the primary lesion that leads to inhibition of root elongation has not been identified. At cellular level, the stimulatory effect of Al on the Fe (II) -dependent peroxidation of lipids has been reported. In cultured tabacco cells, the peroxidation of lipids caused by Al and Fe (II) together is a primary lesion leading to cell death. Under the condition, tobacco cells starved for phosphate (Pi) exhibit tolerance to the toxicity caused by a combination of Al and Fe (II). In addition, we isolated an Al-tolerant cell line (ALT107) from cultured tobacco cells.In this study, we identified antioxidant molecules related to Al tolerance in Pi-starved cells and ALT107 cells as follows :1. Pi-starved cells accumulated carotenoid pigments (especially beta -carotene). In addition, Pi-starved cells, as well as ALT107 cells, accumulated phenylpropanoids including some derivatives of caffeic acid. The phyenylpropanoid compounds protected tobacco cells from the peroxidation of lipids and cell death caused by Al and Fe (II) together, indicating that the phenylpropanoids have antioxidant activity to interfere with the peroxidation of lipids.2. Pi-starved cells and ALT107 cells exhibited an increase in specific activity of phenylalanine ammonia lyase (PAL). Furthermore, a specific inhibitor of PAL completely brocked the accumulation of the phenylpropanoids in Pi-starved cells and ALT107 cells, indicating that PAL is a key enzyme for the accumulation of the phenylpropanoids in cells.These results suggest that the reguglation of the PAL activity is one of the possible mechanism for tolerance to Al toxicity, especially the toxicity caused by Al-enhanced Fe-mediated peroxidation of lipids.